Regulations in thyroid hormone on cardiac protein kinase C signal pathway in vitro

摘要

The experiments were conducted to assess the influences of thyroid hormone on cardiac protein kinase C(PKC) signal pathway with cultured cardiac myocytes and fibroblasts as the models. Cells were pretreated with 1 % newborn calf serum (NCS) or angiotensin II (Ang II), and then following by a triiodothyronine (T3) treatment. The PKC activity, PKCalpha and PKCepsilon expressions were analyzed and compared. In 1 % NCS pretreatment, T3 could inhibit PKC activity and PKCepsilon expression in cardiac myocytes. The AngII pretreatment led to an increase of PKC activity and PKCepsilon expression in cardiac myocytes, and an increase of PKC activity in cardiac fibroblasts. Following by T3 treatment, the increased PKC activity and PKCepsilon expression in cardiac myocytes were markedly decreased. In conclusion, whether in 1 % NCS or in Ang II pretreatment, T3 could inhibit PKC activity and PKCepsilon expression in cardiac myocytes.